CHILDHOOD ASTHMA

dr.Rodman Tarigan, SpA.,MKes

CHILDHOOD ASTHMA

Worldwide In children = the most common chronic disease Account for large proportion of health-care spending, and lost time for school (and work) All medical practisioner should be aware

CHILDHOOD ASTHMA

Over the last decade, research in verious aspect of the biology of asthma are rapidly developing
Certain differences of opnion may exist between authors

CHILDHOOD ASTHMA

DEFINITION MECHANISMS OF DISEASE CLINICAL PRESENTATION PROGNOSIS TREATMENT

DEFINITION I

There is no universally accepted definition

CIBA GUEST SYMPOSIUM, 1959 the condition of subjects with widespread narrowing of the bronchial airways which changes its severity over short periods of time either spontaneously or under treatment..

DEFINITION II

AMERICAN THORACIC SOCIETY (ATS), 1962 :

A disease characterized by an increase responsiveness of the trachea and brochi to various stimuli and manifested by widespread narrowing of.(see CIBA) ATS, 1975: A diseaseand manifested by slowing of forced expiration which changes in severity either

DEFINITION III
WHO, 1975: A chronic condition characterized by recurrent bronchospasm resulting from a tendency to develop reversible narrowing of the airway-lumina in response to stimuli of a level or intensity not inducing such narrowing in most individuals

DEFINITION IV
ATS, 1987: A clinical syndrome characterized by increased responsiveness of tracheobronchial tree to a variety of stimulisymtoms ofparoxysms of dyspnea, wheezing, and cough, which may varyhistologicallyevidence of mucosal edema of the bronchi; infiltration of the bronchial mucosa or submucosa with inflammatory cells, especially eosinophils; and shedding of epithelium and obstruction of peripheral airways with mucus

DEFINITION V
NATIONAL ASTHMA EDUCATION, 1991 A lung disease with following characteristics : 1. Airway obstruction that is reversible either spontaneously or with treatment 2. Airway inflammation 3. Increased airway responsiveness to a variety of stimuli

DEFINITION VI

KONSENSUS UKK-PULMONOLOGI, IDAI, 2000:

batuk dan/atau mengi yang episodik yang telah terbukti bukan disebabkan oleh penyakit lain

MECHANISM OF DISEASE

The exact mechanisms is still unclear

for decades, asthma had been regarded as a classical type I hypersensitivity reaction (IgE triggered release of mast cell mediators intermittent bronchoconstriction)

MECHANISM OF DISEASE

It is now acknowledged that this mechanisms play a very important role but they do not explain recently described biological & clinical features of the disease

MECHANISM OF DISEASE

The factors responsible chronic changes are not well understood. It is likely that different pathogenetic mechanisms may be present in different patients. It is now widely believed that asthma is a heterogeneous disease, with different phenotypes and clinical expressions that depend on age, gender, genetic, background, and environmental exposures.

MECHANISM OF DISEASE

There are 2 main pathogenetic mechanisms responsible for recurrent wheezing during childhood :

1. Altered reactivity to viral infections 2. Allergic airway inflammation

VIRUS Air way epithelial injury

Inflammation
Bronchoconstriction
Mediator cytokines

BHR

Air way narrowing

Sosec factors

Smoking

Age

Wheeze

Host suspect
Immune response Atopy Gen

Viral Resp.Infection and wheezing mechanisms of association

Wheezing associated with allergic airway inflammation

Release of chemotactil mediators: NCF,ECFA. PAF, LTB4
Release lysosomal hydrolase proteoglycans Release of vasoactive mediators: Hist., leukotines, PAF, adenosine, PGD2

Late Asthmatic reaction

Celular infiltrate Activating factors
Eos Neutr Mono T cells Bas Macro

PAF, LTC4

ALLERGEN

Low mol weight Tissue damage repair

Mast cell act. (IgE)

Vasoperbeability smooth muscle contraction

Early Asthmatic reaction

PATHOPHYSIOLOGY
Chemical mediators Bronchoconstriction, mucosal edema, exes.secret Airway obstruction

Atelectasis

Nonuniform ventilation
Mismatching V/P

Hyperinflation
Decreased compliance

Decreased surfactant

Acidosis Pulmonary vasoconstriction

Alveolar Hypoventilation

PaCO2 PaO2

Increased work of breathing

DIAGNOSIS
Mostly can be diagnosed based on data from anamnesis & physical diagnosis
Asthma may have ascribed erroneously to allergic cough, allergic bronchitis, wheezy bronchitis, or chronic bronchitis

DIAGNOSIS
For special cases (asthma varians; asthma with nocturnal-cough), the diagnosis of asthma can be establish with: PEFR/FEV1 before & after bronchodilator Daily-card Bronchial-provocation-test Exercise-testing

ASTHMA
Cough (night) Cough wheezing Wheezing dypsneu Wheezing dypsneu cyanotic

Triggers:, FEV1 <

infection, alergen, < <

Exercise, Weather N <

Bronchospasme

EAR

Bronchospasme +inflammation LAR

BRONCHIAL HYPERACTIVITY

Genetic + Inducer (Infection, Pollution Allergen) ??

CLINICAL MANIFESTATIONS Asthma exacerbation

triggers

symptomless Signs & symptoms of exacerbation: Cough Weezing Tachypnea Dyspnea with prolonged expiration and used of accessory muscles

Signs & symptoms of exacerbation:

Cyanosis Hyperinflation Pulsus paradoxus Abdominal pain due to sternuous use of diaphragm & abdominal muscles Somnolent Barrel chest, harrison sulci Clubbing of the finger

4 CLINICAL VARIATION OF ASTHMA

I Wheezing + Y II

APE X

PEFR (APE) Normal

III

IV

PROGNOSIS

10

15 years

Severe persistent asthma (5%) Moderate persistent astma (20%) Mild asthma (75%)

MANAGEMENT OF CHILDHOOD ASTHMA

BASED ON : ASTHMA = INFLAMATION I. Controlling acute exacerbation II. Preventing acute exacerbation III. Patient and family education

the GOAL: optimal growth and development asthmatic child activity = non asthmatic child

TREATMENT

Basic concepts of avoiding allergens, improving bronchodilation, and reducing mediator-induced-inflamation

Pharmacologic therapy is mainstay of treatment of asthma Consist of relievers (I) controllers (II)

Exacerbation

Relievers

Controllers

II

A. Symphatheticomimethics 1. - Agonist 2. 1-2 Agonist 3. 2 Agonist B. Xantines C. Anticholinergic

MANAGEMENT OF ACUTE EXACERBATION

TO RELIEVE THE CHILD FROM SUFFERING, caused by:

BRONCHOCONSTRICTION COMPLICATION

MANAGEMENT OF ACUTE EXACERBATION

Acute exacerbation
Cough Wheezing Mild dyspneu Moderate dyspneu Severe dyspneu Moderate-severe dyspneu + complication : - Hypoxemia/cyanosis - Acidosis - Respiratory failure - SIADH

DYSPNEU, WHEEZING, PROLONGED EXPIRATION Narrowing bronchial lumina

Bronchospasme

Bronchospasme Inflammation : oedema cell infiltration Hypersecretion

Bronchodilator + Anti-inflammation . Steroid systemic Prednisone Prednisolone Dexamethasone

Bronchodilator
. Simpatetikomimetik . Adrenalin s.c . B-2-agonist s.c., inhalers (salbutamol terbutalin) . Xanthin : Aminofilina I.v. . Anticolinergik : IC, Inhal

CONTROLLING ACUTE EXACERBATION

Early asthmatic reaction = brochospasme

Triggers

Late asthmatic rx =brochospasme + inflammation (oedem, infilt.cell, mukous)

COMPLICATION Hypoxemia Acidosis dehydration Resp. failure Cor-pulm. Atelectasis Bronchiektasis

Avoid from patient

Bronchodilator

Bronchodilator antiinflammation steroid-sytemic

O2 NaHCO3 Fuild 1:4 Ventilator

MILD, MODERATE, SEVERE EXACERBATION O2 , Adrenalin sc/2 agonist

GOOD WheezingDyspneuConscious PARTIAL POOR Wheezing < Dyspneu < Mental status: N

Disccharge - Bronchodilator for 5-7 days

O2 2 agonist nebul every 20 Steroid, po

POOR admitted

GOOD Discharge -Bronchodilator + steroid , po for 5-7 days

MILD, MODERATE, SEVERE EXACERBATION O2 , Adrenalin sc/2 agonist POOR

Wheezing Dyspneu Mental status:

admitted O2 Salbutamol nebulizer every 20 Steroid IVFD 1:4, 5/4 M Bicarbonat Natricus 1-2 mEq/kbBW GOOD Discharge SQA Continue salbutamol WORSE Ventilator

Preventing acute exacerbation

Target: 1. Chronic symptoms << 2. Freq. acute exacerbation << 3. Hospitalized (-) 4. 2- agonist << 5. Sleep and activity disorder (-) 6. Drug side effect (-) 7. APE : normal 8. Daily APE variant < 20 % =====> Indication : Acute exacerbation >1 x /week Night cough > 2 x /month

Thank you